Great concern has been directed toward the development of anti-thrombus agents which can effectively prevent thrombosis-related diseases such as myocardial infarction, cerebral infarction and the like that are of frequent occurrence in recent years. It is known that thromboxane A.sub.2 (TXA.sub.2) which is a strong platelet coagulation factor produced from platelet and the like cells is taking an important role as a cause of these diseases, and that inhibition of its activity is an effective means for the prevention of thrombus formation.
Also, since TXA.sub.2 and other chemical mediators such as leukotriene D.sub.4 (LTD.sub.4) are concerned in allergy, asthma and the like as smooth muscle contraction factors, inhibition of the TXA.sub.2 activity is an effective means for the treatment of late asthma.
Taking such viewpoints into consideration, various TXA.sub.2 synthesis inhibitors and TXA.sub.2 antagonists have been developed, but each having each own problems. For example biosynthesis inhibitors such as Dazoxiben, Ozagrel and the like inhibit a thromboxane synthetase, which by contraries entails accumulation of this enzyme's substrate, prostaglandin H.sub.2 (PGH.sub.2). Similar to the case of TXA.sub.2, PGH.sub.2 itself and other prostaglandins derived from PGH.sub.2, such as PGE.sub.2, are possessed of platelet coagulation and smooth muscle contraction functions. In other words, in spite of the effect of these prior art inhibitors to inhibit TXA.sub.2 production, the inhibition reaction generates coagulation- and contraction-causing substitutes which reduce actual drug effect by half. On the other hand, TXA.sub.2 antagonists such as S-145, Daltroban and the like compete with the TXA.sub.2 receptor which exists in platelets. Because of such a reaction mechanism, these antagonists exhibit effective TXA.sub.2 inhibition activity by competing with the receptor when the amount of produced TXA.sub.2 is small, but their efficacy decreases as the amount of produced TXA.sub.2 increases. In such a case, therefore, it is necessary to inhibit TXA.sub.2 production itself. In addition, TXA.sub.2 antagonists are not concerned in the production of prostaglandin PGI.sub.2 which has anti-thrombotic activity.